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→Pathophysiology of Shock
==Pathophysiology of Shock==
==Pathophysiology of Shock==
In shock caused by haemorrhage or burns, there is reflex vasoconstriction of the peripheral and splanchnic blood vessels. The body becomes starved of oxygen but there is no constriction of the cerebral or coronary blood vessels - this protects the brain and the heart.
The fall in blood pressure stimulates the release of renin from the kidney; consequently angiotensin from the liver is activated which causes an increase in blood pressure. This in turn stimulates the adrenal cortex to secrete aldosterone, which causes the kidney to retain sodium and water.
The kidney is particularly vulnerable to shock; the flow of urine may cease and if the condition is prolonged, acute tubular necrosis can develop.
* After a sustained period of oxygen deficit, the vasomotor control over the blood vessels is lost. Blood becomes pooled in the capillary beds and this state is termed "irreversible shock" which is rapidly fatal.
* After a sustained period of oxygen deficit, the vasomotor control over the blood vessels is lost.
==Post-Mortem Findings==
==Post-Mortem Findings==